1. Field of the Invention
The present invention relates to the field of treating or preventing tissue deterioration, injury or damage due to periodontal disease or disease of oral mucosa, and/or downregulating or suppressing NF-kappaB-mediated actions in a body.
2. Description of the Background Art
NF-kappaB is the prototype of a family of dimeric transcription factors made from monomers that have approximately 300 amino-acid Rel regions which bind to DNA, interact with each other, and bind the I kappaB inhibitors. Activation of NF-kappaB to move into the nucleus is controlled by the targeted phosphorylation and subsequent degradation of I kappaB. There are multiple forms of I kappa B that appear to regulate NF-kappaB by distinct mechanisms. NF-kappaB can be activated by exposure of cells to LPS or inflammatory cytokines such as TNF or IL-1, viral infection or expression of certain viral gene products, UV irradiation, B or T cell activation, and by other physiological and nonphysiological stimuli. NF-kappaB activation has been implicated in many biological processes, including inflammation, immunoregulation, apoptosis, neuronal function, cell growth and transportation, and cell proliferation.
Inflammatory responses are a major component of secondary injury and play a central role in mediating the pathogenesis of acute and chronic spinal cord injury (SCI). The nuclear factor-kappaB (NF-kappaB) family of transcription factors is required for the transcriptional activation of a variety of genes regulating inflammatory, proliferative, and cell death responses of cells. NF-kappaB activation occurs as early as 0.5 hr postinjury and persists for at least 72 hr. Activated NF-kappaB has been detected in macrophages/microglia, endothelial cells, and neurons within the injured spinal cord. Colocalization of activated NF-kappaB with the NF-kappaB-dependent gene product, inducible nitric oxide synthase (iNOS), suggests functional implications for this transcription factor in the pathogenesis of acute spinal cord injury.
Periodontal (gum) diseases, including gingivitis and periodontitis, are serious infections that, left untreated, can lead to tooth loss. Periodontal disease can result from chronic bacterial infection that affects the gums and bone supporting the teeth.
Periodontal disease can affect one tooth or many teeth. It often begins when the bacteria in plaque causes the gums to become inflamed.
Gingivitis is the mildest form of periodontal disease. It causes the gums to become red, swollen, and bleed easily. There is usually little or no discomfort at this stage.
Untreated gingivitis can advance to periodontitis. With time, plaque can spread and grow below the gum line. Toxins produced by the bacteria in plaque irritate the gums. The toxins stimulate a chronic inflammatory response in which the body in essence turns on itself, and the tissues and bone that support the teeth are broken down and destroyed. Gums separate from the teeth, forming pockets (spaces between the teeth and gums) that become infected. As the disease progresses, the pockets deepen and more gum tissue and bone are destroyed. Often, this destructive process has very mild symptoms. Eventually, teeth can become loose and may have to be removed.
Periodontitis as a Manifestation of Systemic Diseases are forms of periodontal disease which often begin at a young age, associated with one of several systemic diseases, such as diabetes.
Necrotizing Periodontal Diseases are forms of periodontal disease which are infections characterized by necrosis of gingival tissues, periodontal ligament and alveolar bone. These lesions are most commonly observed in individuals with systemic conditions including, but not limited to, HIV infection, malnutrition and immunosuppression.
Aggressive Periodontitis is a form of periodontitis that occurs in patients who are otherwise clinically healthy. Common features include rapid attachment loss and bone destruction and familial aggregation.
Chronic Periodontitis is a form of periodontal disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment and bone loss and is characterized by pocket formation and/or recession of the gingiva. It is recognized as the most frequently occurring form of periodontitis. It is prevalent in adults, but can occur at any age. Progression of attachment loss usually occurs slowly, but periods of rapid progression can occur.
Up to 30% of the population may be genetically susceptible to gum disease. Despite aggressive oral care habits, these people may be six times more likely to develop periodontal disease.
There remains a need in the art for methods of treatment for treating, preventing, inhibiting or reducing tissue deterioration, injury or damage due to periodontal disease or disease of oral mucosa and/or influencing activities of NF-kappaB in a body.